Stimulation of the BKCa channel in cultured smooth muscle cells of human trachea by magnolol

Abstract

Background: Magnolol, a compound isolated from the cortex of Magnolia officinalis, has been found to possess anti-allergic and anti-asthmatic activity. Methods: The effect of magnolol on ionic currents was studied in cultured smooth muscle cells of human trachea with the aid of the patch clamp technique. Results: In whole cell current recordings magnolol reversibly increased the amplitude of K + outward currents. The increase in outward current caused by magnolol was sensitive to inhibition by iberiotoxin (200 nM) or paxilline (1 µM) but not by glibenclamide (10 µM). In inside out patches, magnolol added to the bath did not modify single channel conductance but effectively enhanced the activity of large conductance Ca 2+ activated K + (BK Ca ) channels. Magnolol increased the probability of these channel openings in a concentration dependent manner with an EC 50 value of 1.5 µM. The magnolol stimulated increase in the probability of channels opening was independent of internal Ca 2+ . The application of magnolol also shifted the activation curve of BK Ca channels to less positive membrane potentials. The change in the kinetic behaviour of BK Ca channels caused by magnolol in these cells is the result of an increase in dissociation and gating constants. Conclusions: These results provide evidence that, in addition to the presence of antioxidative activity, magnolol is potent in stimulating BK Ca channel activity in tracheal smooth muscle cells. The direct stimulation of these BK Ca channels by magnolol may contribute to the underlying mechanism by which it acts as an anti-asthmatic compound.

Signaling pathway of magnolol‐stimulated lipolysis in sterol ester‐loaded 3T3‐L1 preadipocyes

“…Magnolol relaxed rat thoracic smooth muscle cells by inhibiting calcium influx through voltage-gated calcium channels [Teng et al, 1990], whereas it stimulated BK (Ca) channel activity in human tracheal smooth muscle cells [Wu et al, 2002]. Induction of [Ca 2þ ] i elevation by magnolol was found to be phospholipase C-dependent manner in human hepatoma and colon cancer cell lines or inositol triphosphate signaling pathway in rat neutrophils [Wang and Chen, 1998].…”

Magnolol blocks homocysteine-induced endothelial dysfunction in porcine coronary arteries

“…Studies have shown that magnolol can reduce myocardial ischemia-reperfusion injury via neutrophil inhibition in rats (Lee et al, 2001) and can reduce coronary restenosis in animal model (Serruys, Foley, Kirkeeide, & King, 1993). Magnolol was considered a candidate drug for alleviating restenosis via inhibition of vascular smooth muscle cell (VSMC) proliferation (Wu et al, 2002). In the present study, we investigated the vasodilator effect of magnolol and found that it is an effective vasodilator.…”

Magnolol encapsulated by different acyl chain length of liposomes on inhibiting proliferation of smooth muscle cells

“…The past research revealed that magnolol had two kinds of different functions (Han et al, 2007;Kuntz and Baim, 1993). Magnolol was not only expected to apply in inhibiting retenosis of smooth muscle cells proliferation but also as a pharmacological approach for restenosis by inhibiting vascular smooth muscle cells (VSMCs) proliferation (Hong et al, 1996;Wu et al, 2002Wu et al, , 2005.…”